Wallis Christopher M, Gorman Zachary, Galarneau Erin R-A, Baumgartner Kendra
Crop Diseases, Pest and Genetics Research Unit, San Joaquin Valley Agricultural Sciences Center, United States Department of Agriculture (USDA)-Agricultural Research Service, Parlier, CA, United States.
Plant Genetics Resources Unit, USDA-Agricultural Research Service, Geneva, NY, United States.
Front Fungal Biol. 2022 Sep 15;3:1001143. doi: 10.3389/ffunb.2022.1001143. eCollection 2022.
As grapevines mature in California vineyards they accumulate chronic wood infections by the Ascomycete fungi that cause trunk diseases, including Botryosphaeria dieback (caused by and ) and Esca (caused by ). It is thought that such mixed infections become localized to separate internal lesions/cankers of the permanent, woody structure of an individual vine, but nonetheless the fungi all colonize the same vascular system. In response to infection by one pathogen, the host may initiate systemic biochemical changes, which in turn may affect the extent of subsequent infections by other pathogens. To test this hypothesis, we measured changes in phenolic compounds in the wood and lesion lengths of the pathogens, during sequential co-inoculations with different or identical pair-wise sequences of infection by , , or . Prior fungal infections only affected the development of subsequent infections. Effects of fungal infections on phenolic compounds were variable, yet initial infection by was associated with significantly higher concentrations of most phenolic compounds distally, compared to all other initial inoculation treatments. It was hypothesized that pre-existing phenolic levels can slow initial lesion development of fungal trunk pathogens, especially for , but over time the pathogens appeared to overcome or neutralize phenolic compounds and grow unimpeded. These results demonstrate that effects of one fungal trunk pathogen infection is generally unable to distally affect another long-term, albeit shifts in host phenolics and other plant defenses do occur.
在加利福尼亚的葡萄园里，随着葡萄树的成熟，它们会受到子囊菌的慢性木质部感染，这些子囊菌会引发树干病害，包括葡萄座腔菌溃疡病（由 和 引起）和埃斯卡病（由 引起）。据认为，这种混合感染会局限于单个葡萄树永久性木质结构的不同内部病斑/溃疡，但真菌都会定殖于同一个维管系统。针对一种病原体的感染，宿主可能会启动系统性的生化变化，这反过来可能会影响后续其他病原体的感染程度。为了验证这一假设，我们在依次共同接种 、 或 的不同或相同两两组合感染序列期间，测量了木材中酚类化合物的变化以及病原体的病斑长度。先前的真菌感染仅影响后续 感染的发展。真菌感染对酚类化合物的影响各不相同，但与所有其他初始接种处理相比，最初由 感染与远端大多数酚类化合物的显著更高浓度相关。据推测，预先存在的酚类水平可以减缓真菌树干病原体的初始病斑发展，特别是对于 ，但随着时间的推移，病原体似乎能够克服或中和酚类化合物并不受阻碍地生长。这些结果表明，一种真菌树干病原体感染的影响通常无法在远端长期影响另一种病原体，尽管宿主酚类物质和其他植物防御确实会发生变化。
